It’s like this, the synergistic relationship between opiate pain relievers and cannabis has been anecdotally noted by western physicians from around 1850 until… Well, now that I think on it, I suppose docs are still seeing similar results in some patients.

The research study performed by Wilson-Poe, Morgan, Aicher and Hegarty (right here at WSU, Vancouver!) gives us a clue how that works from a biological standpoint. I love this stuff, man. Have I already told you that?

We’re all hip to the synapse/key thing, right? Agonists and antagonists? The analogy is, certain molecules act like keys tripping the locks in neurons. The agonist is responsible for the resulting electrical potential to momentarily… the nerve “fires,” okay? Toss a wad of putty into the key hole and the antagonist stands there giving you the raspberries. Nothing happens.

In this study the THC synthetic used was HU-210. Researchers are forced to use synthetic cannabinoids because the real stuff is, you know? – against the law.

They tell us the PAG (grey brain matter) has a lot to do with pain sensation (antinociception). They say if you pump a little cannabinoid into the gray matter, then less morphine is required to get the same result as you’d get without the cannabinoid.

Their work gives us a good insight as to why. Though, I’ll admit to a bit of confusion near the conclusion.

A MOP (mu) receptor is an opioid receptor. Dorsolateral and ventrolateral are simply location. Immunocytochemical means they’ve “tagged” cells for identification. Somatodendritic just means there are receptors on both the cell body (soma) and on the tentacle looking things called dendrites.

That big red part with all of the cool different colored patterns in it would be the soma. Notice the flesh-colored dendrite (above the red) interfaces not only on the other dendrite, but on the soma as well. Cool.

Okay, now here is where I get a bit confused. I think what they’re telling us is 8% of the cells analyzed had both opioid and cannabis receptors. Pretty sure. If that’s the case then it would explain the synergy, eh? I mean, if a cannabinoid has a bunch of cells reacting already, then less opiate is required for the desired result. That’s pretty easy to grasp. I guess.

I dunno, I’m no rocket surgeon.

“These results indicate that behavioral interactions between cannabinoids and opioids may be the result of cellular adaptations…”

I’d like to see a similar study, only using methanandamide (synthetic ananamide) or 2-AG in place of HU-210. Anandamide and 2-AG are endocannabinoids – stuff our bodies manufacture.

This study gives us some idea how the relationship between opiates and cannabinoids operates at the cellular level. Very cool, eh?